The Nutrition Debate #305: My Troubled Relationship with Food

This is a hard thing to admit, but easy to see, if you know me. While I am still 110 pounds lighter than I was in 2002, I am 60 pounds heavier than I was at my lowest in 2008, and that’s no accident. I ate myself that way, and today I am, in fact, still fat. Technically, with a Body Mass Index (BMI) of 37, I am considered obese. And even at my lowest weight (204 pounds), my BMI (28.5) was still at the high end of overweight! How did the weight regain happen? Well, I’ll tell you.

Before I do, though, I want you to know that I am, I think – and I think my doctor would agree – much, much healthier than I was in 2002. And I don’t mean just less fat. I have a much better and more stable blood sugar level, and I have been able to give up and stay off virtually all of the oral anti-diabetic medications I was taking back then. My Type 2 diabetes is still “in remission,” although my fasting blood sugars are usually “pre-diabetic” (>100mg/dl <126mg/dl), as are my A1c’s (high 5s). But my cholesterol profile has dramatically improved, with HDLs doubled and triglycerides cut by 2/3rds. See my popular blog posts # 281, #282 and #283 for a 35-year history with charts. And my hs CRP’s, chronic systemic inflammation markers, are very much improved (usually <1.0mg/dl, down from +/-6mg/dl). And – (drum roll) – my doctor took me off statins years ago.

And why is that? Why all the good news while I have re-gained 35% of my original weight loss? It is because I have fundamentally changed what I (usually) eat. I still follow a low-carb, high-fat (LCHF) Way of Eating most of the time. But I “cheat.” I’ll sometimes scarf down rolls (with butter) brought to the table in a restaurant. Sure, we could say, “no bread,” and sometimes we do, but at other times we don’t. I also raid the freezer at home occasionally to steal some of my wife’s ice cream. You see how easy it is to “blame” someone else for mytransgressions. At least I recognize the self-delusion.

It would also be easy to blame “habituation to rewarding neural dopamine signaling [that] develops with the chronic overconsumption of palatable foods, leading to a perceived reward deficit and compensatory increases in consumption.” For a good scientific roundup of why obesity is a vexing problem, see The Nutrition Debate #297: “Obesity in Remission.”

How things now stand: Because I eat LCHF, for the most part my Type 2 Diabetes continues to be in remission. But because I have lost a great deal of weight, I also have Obesity in Remission. As a consequence I need always to remember to “eat healthy” and at least 20% less than someone who has not previously been fat. “Elections have consequences,” and since I elected to eat carbs in excess and developed carbohydrate intolerance, I am foreverpredisposed to accumulate excess fat.

But 1) if I eat only the foods I have espoused and recognized as “good” for me, and 2) if I only eat when I am hungry, or alternatively just two small meals a day instead of the conventional three, I believe a) I would not have gained back any weight, and b) I might have continued to lose weight. After all, I probably shouldn’t weigh, at most, more than 175 pounds (BMI=24). But I did and I do, and so I confess it. Will that do me (or you, for that matter) any good? Well, the first step in making a change in your life is to acknowledge what you are doing that needs to change. And now I’ve done that.

So, we’ll see. I’m going to take a break now from writing this blog. I’ve written 305 posts over the last 4 years and 5 months. They have received altogether more than 150k page views, so it’s likely that someone (besides me) has benefitted from them. Readers who want to keep in touch, while I return to basics, can write to danbrown@thenutritiondebate.com. Or, visit the Bernstein Diabetes Forum, where I post from time to time and there’s lots of other friendly help and support and very good advice, especially for Type 2s and pre-diabetics who want to manage their condition with the aim of avoiding “the current treatment protocols (that) trap patients in a lifelong regimen of drug management, obesity and escalating diabetes.”

In taking leave of my readers I would be remiss if I didn’t heap praise on my editor. She has been a stalwart friend and helper throughout this period, always there with timely and helpful edits and links to scholarly resources. She is an inveterate professional, a tireless fact checker and my overall guiding support. And - no contest here – she always knew the subject better than I did. Thank you, thank you, and thank you, Laurie Weakley. (Too many “thank you’s,” Laurie?)

The Nutrition Debate #304: “I am not making this up”

“Novel differences in the glucose response to HP [higher-protein] vs. NP [normal-protein] breakfasts were observed and were influenced by the frequency of habitual breakfast consumption in overweight adolescents.” At 176 characters (with spaces), it might have made a good tweet. But, and I am not making this up, that was the CONCLUSION from the Abstract of a recent article in the European Journal of Clinical Nutrition (EJCN). I saw the groundbreaking news from Diabetes in Control: “Breakfast Habits Affect Overweight Teen Girls Metabolic Responses to Protein-Packed Morning Meals.”

“The primary aim [of the study] was to examine the daily glycemic response to normal-protein (NP) vs. higher-protein (HP) breakfasts in overweight adolescents who habitually skip breakfast (H-BS). The secondary aim examined whether the glycemic response to these meals differed in H-BS vs. habitual breakfast consumers (H-BC),” according to the EJCN. If this sounds elementary, Watson, I’ll generously assume the research was intended to educate overweight/obese late adolescent girls in an online chat line or similar social media or some teen-oriented supermarket magazine.

The unsurprising outcome was that “those who typically ate a high-carbohydrate breakfast had improved glucose control after they ate a high-protein breakfast.” No news there. But the researchers seemed surprised that “the habitual breakfast skippers experienced poorer glycemic control throughout the day when they consumed a high protein breakfast.” Hmmm. Ingested food affects your circulating blood glucose! It disrupts and destabilizes it! It causes glucose, from carbs and then from protein digestion via gluconeogenesis over 4 or 5 hours, to enter your bloodstream, resulting in peaks and crashes!

The Abstract (you have to pay to access the full paper) does not tell us what a “normal protein” breakfast is (as compared to a higher-protein breakfast) but you can bet it contains lots of carbs too: juice, cereal and/or some bread product.

“These findings may indicate an increased inability among habitual breakfast skippers to metabolize a large quantity of protein,” the corresponding researcher told Diabetes in Control. “However, our data would suggest that once someone begins to eat breakfast, they should gradually transition to a breakfast with more protein – or about 30 grams – to elicit improvements in glycemic control,” the researcher said. Wow! That (30g) is a lot of protein. They must be growing girls.

I think the education of the researcher is proceeding swimmingly. The paper stipulates, “Current scientific evidence shows that sustained elevations in post-meal glucose is a strong contributor of poor glycemic control and is associated with an increased risk for the development of Type 2 diabetes and cardiovascular complications. Because of the potential risk in the long term, identifying dietary strategies that individuals can begin when they are young to reduce post-meal elevations in glucose might prevent the occurrence of Type 2 diabetes and cardiovascular disease.” That’s a safe bet. And well said!

According to the Diabetes in Control write-up, the researcher suggested that “young women should routinely aim for a 350-calorie breakfast with approximately 30 grams of protein. To meet the recommended 30 grams of protein, [the researcher] suggests foods such as scrambled eggs, breakfast burritos with eggs and lean meats, or Greek Yogurt.” Interesting, my breakfast is 3 eggs, fried or scrambled, 1 strip of bacon, a large coffee with stevia powder and about 4 Tbs of half and half, and a 1 gram fish oil capsule. It’s 375 calories, but only 20 grams of protein, 31 grams of fat and 4 grams of carbs.

I also think the researcher needs to take another look at 1) gluconeogenesis and 2) the “standard lunch” the girls ate. But progress, progress.

The Nutrition Debate #303: Poor Dr. Walter Willett

The Nutrition Source, not to be confused with The Nutrition Debate (teehee), is the Harvard T. H. Chan School of Public Health’s website. Its aim is “to provide timely information on diet and nutrition for clinicians, allied health professionals, and the public.” I took a poke at their Alternate Healthy Eating Index last year in The Nutrition Debate #229 with “My Alternate Healthy Eating Index.” To their credit, they do bring to the table some gravitas, in my view, because they deign to criticize the USDA’s Dietary Guidelines, as the HSPH’s Alternate Healthy Eating Index amply demonstrates.

Much of that gravitas is attributable to Dr. Walter Willett, Professor of Epidemiology and Nutrition and chairman of the HSPH; he’s also professor of medicine at the Harvard Medical School’s teaching hospital, Brigham and Women’s. Willett is “the principal investigator of the second Nurses' Health Study, a compilation of studies regarding the health of older women and their risk factors for major chronic diseases. He has published more than 1,000 scientific articles regarding various aspects of diet and disease and is the second most cited author in clinical medicine,” according to Wiki.

Staying “King of the Hill” can be a rough game. Ancel Keys, despite numerous attempts to dethrone him, stayed King until long after he was smoldering in the grave. In fact, his ghost still casts a ghoulish pale. And Walter Willett has recently managed to do so too, using the same type of rough play as Keys used. This 2013 piece in Forbes tells the story of how the “Top Science Journal Rebukes Harvard’s Top Nutritionist.” The Nature story and accompanying editorial were both scathing. Willett’s offense was to say on NPR that a research piece in JAMA by Katherine Flegal, that showed people who were overweight (but not obese) lived longer than those deemed normal weight, was “a pile of rubbish, and no one should waste their time reading it.” He then organized a conference at Harvard expressly to discredit the JAMA piece.

More recently, Nina Teicholz, author of “The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet,” wrote a New York Times op-ed, “The Government's Bad Dietary Advice.” In it she says, “…the primary problem is that nutrition policy has long relied on a very weak kind of science: epidemiological, or “observational,” [i.e. “cohort”] studies in which researchers follow large groups of people over many years. But even the most rigorous epidemiological studies suffer from a fundamental limitation. At best, they can only show an association, not causation.”

“Epidemiological studies can be used to suggest hypotheses but not to prove them,” Teicholz said. “Instead of accepting that this evidence was inadequate to give sound advice, strong-willed scientists [ahem] overstated the significance of their studies.” Then, she zeros in: “Much of the epidemiological data underpinning the government’s dietary advice comes from studies run by Harvard’s school of public health.” Teicholz doesn’t pull punches. She also takes a hit at the Guideline’s advice on salt by citing a blistering and “authoritative Institute of Medicine study.” I cite it in #153: “Salt: Friend or Foe.” See also Medscape Medical News Editor-in-Chief Eric Topol’s report in #248, “Salt Warnings: Confusing and Contradictory.”

Now, Dr. Willett has used his quarterly, “Ask the Expert” interview to address the cholesterol issue. (Note: the draft 2015 Dietary Guidelines, for the first time since 1980, states that “cholesterol is not considered a nutrient for overconsumption.”) Largely responding to the Teicholz guest op-ed (that he inexplicably calls the NYT “story” or “article”), Willett says,

“The important point is to have the best possible evidence, and we shouldn’t be basing dietary guidance on just guesses or beliefs. In the case of both the egg issue and the total fat issue we were basically starting with virtually no direct evidence. When the evidence did start to come in – and there were different lines of evidence from our studies based on large cohorts and also short term studies investigating metabolic changes – it showed that people who consume more eggs did not have a higher risk of heart disease even after adjusting for any other factors, and that total fat in the diet was not related to heart disease risk or cancer risk. So it took those long term studies to show that those were not important factors, and that allowed us to modify the recommendations. We were really in a state 35 years ago in which we had very little direct evidence and we were basing guidelines on guesses and indirect evidence from very small, short term studies.”

Mea culpa? Mea culpa!!!!! But I think the best rebuke of Willett is from the Forbes piece. You have to read the story for context, but this sums it up well. This is “piling on,” of course, but sometimes that’s the best way with King of the Hill.

“Science is complex, and Willett’s message to his fellow scientists appears to be that the public can’t be trusted with this complexity (except, as noted, when it might be something that he thinks is worthy of research); the question, which the public might ask in turn, is whether Willett can be trusted with complexity given his apparent intolerance for it in other scientists?”

The Nutrition Debate #302: Another pill to prevent Type 2 Diabetes?

As everyone who regularly reads this blog knows, I am not a pill pusher. I once was a big-time pill-taker, however, until I tried an alternative “treatment plan” for my Type 2 diabetes. I was a passive victim of “the current treatment protocols (that) trap patients in a lifelong regimen of drug management, obesity and escalating diabetes” (see #292 here). 

That stopped when my doctor “prescribed” a total change of diet, to lose weight,which had the added effect of putting my diabetes in clinical remission. I went from being maxed out on 2 oral diabetes meds and starting a 3rd (with an out of control FBG) to where I am today, taking 1 low-dose Metformin and good glucose control. My A1c’s are always in the 5s.

But this blog is not about Very Low Carb dieting. It is about an interesting new idea (for me) from some Danish researchers, according to this Diabetes in Control story. It is based on “a large study population of adults (lean and obese, men and women) with normal and impaired glucose regulation.” They are from the Steno Diabetes Center, a Danish hospital and research organization owned by the drug maker Novo-Nordisk, “working in partnership with the Danish healthcare system.”

The FINDING, which could prove to be significant: “Reduction in the glucose-regulating hormone glucogon-like-peptide-1 (GLP-1) appears to occur before the development of type 2 diabetes and obesity," according to the abstract in Diabetes.

The lead investigator told Diabetes in Control, “We found that GLP-1 is reduced by up to 25% among people with pre-diabetes and up to 20% among obese people compared to normal-weight people. This indicates that the reduction in GLP-1 is not a consequence of type 2 diabetes, but appears much earlier in the disease development and may predispose people to type 2 diabetes.” These results were all in response to an oral glucose tolerance test (OGTT).

The Diabetes in Control piece also noted, “And what is surprising is that they have also found pronounced differences in GLP-1 secretion between men and women. They observed a higher GLP-1 response among women than men, but when glucose tolerance worsens, the decline in GLP-1 secretion is more pronounced in women than in men.”

Of course, as might be expected from a hospital research department “owned by Novo Nordisk, working in partnership with the Danish healthcare system,” the researchers casually said, “‘These results could have potential clinical implications as well,’ noting that GLP-1 analogs may help delay onset of type 2 diabetes,” Diabetes in Control noted. A GLP-1 analog would be a new drug designed “to prevent diabetes for those with prediabetes.” And…for overweight and obese patients too?

They may be on to something here. Preventing the destruction of GLP-1 would be a worthy area for further investigation. But, alternatively, developing a new drug, a GLP-1 analog, to treat the symptom rather than the cause – something that Big Pharma, working in partnership with the…healthcare system (government funding) does so well – is a sure fire hit. It sounds like a big money maker (for Novo Nordisk) to me. Think statins, or blood pressure medications, or any other of “the current treatment protocols (that) trap patients in a lifelong regimen of drug management.”

Hey, I believe in capitalism, and Novo Nordisk is not an eleemosynary enterprise. They have a pecuniary interest in this research. So, let’s hope the researchers are sincere when they say, according to their press release, “We should use the findings in prevention strategies for type 2 diabetes.” Sounds good. More studies. In the meantime, eat Very Low Carb! Preserve your GLP-1!

The Nutrition Debate #301: Healthy Food Choices

Unfortunately, this catch phrase has been co-opted and misused by our government’s “Dietary Dictocrats” to mean mostly things that I and like thinkers consider unhealthy food choices, like highly processed vegetable oils. It has also been used to denigrate saturated fat and, until the present iteration of the much anticipated 2015 Dietary Guidelines for Americans, dietary cholesterol. (In case you haven’t heard, cholesterol has been declared “no longer a nutrient of concern for overconsumption.”) If you searched for the USDA’s idea of “healthy food choices,” you should stop reading this now…or, maybe continue reading. You might learn something.

Healthy food choices, in the sense that I mean, are whole, unprocessed foods, including lots of animal-based proteins and fats, together with fresh, whole, low-carb vegetables (mostly of the above-ground grown type), and an occasional berry (with heavy cream) and a few nuts (added to salads, e.g.). It involves the almost complete avoidance of grains, and processed foods made from flour and sugars (cane, beet or corn) and all processed vegetable oils. So, among my healthy food choices, what other choices can I (we) make to be healthier?

Eggs from pastured hens: This was an easy choice. We have, at our farmers’ market, a farmer who raises hens in the manner of Joel Salatin’s Polyface Farm in Virginia, made famous by Michael Pollan’s “Omnivore’s Dilemma.” The hens roam freely and roost in a portable hen house that is towed around every week or two to pastures in which the farm’s ruminants (and pigs) had grazed and left “deposits” to fertilize the fields and nourish the hens. Chickens (and pigs) are omnivores, so the hens get a balanced diet including bugs and, from aged patties, larvae.

Butter from pastured cows: It stands to reason that cows that are fed, during part or all of the year, a diet of mostly silage, will produce milk, cream and butter that have fewer nutrients.  Is it not better for ruminants to eat natural forage instead of fodder? Laboratory tests of milk and butter have confirmed this. Grass-fed cows produce milk and butter that is higher in vitamins, minerals and other essential nutrients like Omega 3 fatty acids. Is it not then a better choice to choose butter made from cows that are grazed on forage all year round? I’m going to start buying butter made from grass-fed cows and ask my wife to use it instead of the store brand.

Wild Caught versus Farm Raised Fish: Of course, I eat wild-caught fish almost every day (a can of sardines for lunch), but choosing wild-caught fresh or flash-frozen fish from the supermarket or fish monger’s case is an easy choice to adopt. Some fish like North Pacific salmon must be wild-caught, but beware of farm-raised salmon from the North Atlantic or South Pacific (Chile). Other types of fish – cod, for example, one of the less expensive species, is always wild-caught and is a white, flaky, non-fishy tasting fish. I make a stove-top recipe with fennel and cauliflower. Halibut with celery, also stovetop, is another tasty wild-caught choice dish. Why not try them?

Lamb chops: Lamb chops, though expensive, are a very good fatty meat choice for a couple of reasons. Most lamb is raised in New Zealand, where they are grass-fed year round. They are not feed-lot raised. And they are ruminants, so they are a good choice for their fatty acid profile (better than chickens and swine). And, since lamb chops are small, they make portion control easy. My wife and I eat just two lamb chops each – about 4 to 6 ounces net – making a perfect protein portion for a supper where my “allowance” is just 25 grams of protein.

Heritage Pork: Supermarket pork, “the other white meat” has had all the healthy fats bred out of it. Supermarket pork chops taste like sawdust unless they are smothered in gravy (ugh!). You just can’t get away from how dry they are. The answer is to buy heritage breed pork. Breeds to look for are: Berkshire, Tamworth, and Red Wattle. Again, your local farmers’ market is the place to look for these superior tasting products, especially roasts. 

Artificial Sweeteners: I have finally weaned myself off artificial sweeteners. I used to take Splenda in my coffee and to sweeten the unsweetened Lipton’s ice tea we drink (instead of water!). Now I use pure stevia leaf extract, a powder with no bulking agents. I understand that stevia is also available as a liquid. I do not know the solvent.